http://purl.uniprot.org/citations/11015443 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11015443 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11015443 | http://www.w3.org/2000/01/rdf-schema#comment | "PD-1 is an immunoinhibitory receptor expressed by activated T cells, B cells, and myeloid cells. Mice deficient in PD-1 exhibit a breakdown of peripheral tolerance and demonstrate multiple autoimmune features. We report here that the ligand of PD-1 (PD-L1) is a member of the B7 gene family. Engagement of PD-1 by PD-L1 leads to the inhibition of T cell receptor-mediated lymphocyte proliferation and cytokine secretion. In addition, PD-1 signaling can inhibit at least suboptimal levels of CD28-mediated costimulation. PD-L1 is expressed by antigen-presenting cells, including human peripheral blood monocytes stimulated with interferon gamma, and activated human and murine dendritic cells. In addition, PD-L1 is expressed in nonlymphoid tissues such as heart and lung. The relative levels of inhibitory PD-L1 and costimulatory B7-1/B7-2 signals on antigen-presenting cells may determine the extent of T cell activation and consequently the threshold between tolerance and autoimmunity. PD-L1 expression on nonlymphoid tissues and its potential interaction with PD-1 may subsequently determine the extent of immune responses at sites of inflammation."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.org/dc/terms/identifier | "doi:10.1084/jem.192.7.1027"xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.org/dc/terms/identifier | "doi:10.1084/jem.192.7.1027"xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Okazaki T."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Okazaki T."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Collins M."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Collins M."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Nishimura H."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Nishimura H."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Carter L."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Carter L."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Honjo T."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Honjo T."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Freeman G.J."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Freeman G.J."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Ling V."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Ling V."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Chernova T."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Chernova T."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Iwai Y."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Iwai Y."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Long A.J."xsd:string |
http://purl.uniprot.org/citations/11015443 | http://purl.uniprot.org/core/author | "Long A.J."xsd:string |